| Structural highlights
Function
[RCD1_ARATH] Inactive ADP-ribosyltransferase that functions with SRO1 to regulate oxidative stress, hormonal and developmental responses. Required for embryogenesis, vegetative and reproductive development, and abiotic stress responses. May regulate several stress-responsive genes. Seems to play a larger developmental role than SRO1. Does not bind NAD in vitro.[1] [2] [3] [4] [5] [6] [7] [8] [9] [10]
Publication Abstract from PubMed
The oomycete pathogen Hyaloperonospora arabidopsidis (Hpa) causes downy mildew disease on Arabidopsis. To colonize its host, Hpa translocates effector proteins that suppress plant immunity into infected host cells. Here, we investigate the relevance of the interaction between one of these effectors, HaRxL106, and Arabidopsis RADICAL-INDUCED CELL DEATH1 (RCD1). We use pathogen infection assays as well as molecular and biochemical analyses to test the hypothesis that HaRxL106 manipulates RCD1 to attenuate transcriptional activation of defense genes. We report that HaRxL106 suppresses transcriptional activation of salicylic acid (SA)-induced defense genes and alters plant growth responses to light. HaRxL106-mediated suppression of immunity is abolished in RCD1 loss-of-function mutants. We report that RCD1-type proteins are phosphorylated, and we identified Mut9-like kinases (MLKs), which function as phosphoregulatory nodes at the level of photoreceptors, as RCD1-interacting proteins. An mlk1,3,4 triple mutant exhibits stronger SA-induced defense marker gene expression compared with wild-type plants, suggesting that MLKs also affect transcriptional regulation of SA signaling. Based on the combined evidence, we hypothesize that nuclear RCD1/MLK complexes act as signaling nodes that integrate information from environmental cues and pathogen sensors, and that the Arabidopsis downy mildew pathogen targets RCD1 to prevent activation of plant immunity.
Arabidopsis downy mildew effector HaRxL106 suppresses plant immunity by binding to RADICAL-INDUCED CELL DEATH1.,Wirthmueller L, Asai S, Rallapalli G, Sklenar J, Fabro G, Kim DS, Lintermann R, Jaspers P, Wrzaczek M, Kangasjarvi J, MacLean D, Menke FLH, Banfield MJ, Jones JDG New Phytol. 2018 Oct;220(1):232-248. doi: 10.1111/nph.15277. PMID:30156022[11]
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.
See Also
References
- ↑ Belles-Boix E, Babiychuk E, Van Montagu M, Inze D, Kushnir S. CEO1, a new protein from Arabidopsis thaliana, protects yeast against oxidative damage. FEBS Lett. 2000 Sep 29;482(1-2):19-24. PMID:11018516
- ↑ Overmyer K, Tuominen H, Kettunen R, Betz C, Langebartels C, Sandermann H Jr, Kangasjarvi J. Ozone-sensitive arabidopsis rcd1 mutant reveals opposite roles for ethylene and jasmonate signaling pathways in regulating superoxide-dependent cell death. Plant Cell. 2000 Oct;12(10):1849-62. PMID:11041881
- ↑ Fujibe T, Saji H, Arakawa K, Yabe N, Takeuchi Y, Yamamoto KT. A methyl viologen-resistant mutant of Arabidopsis, which is allelic to ozone-sensitive rcd1, is tolerant to supplemental ultraviolet-B irradiation. Plant Physiol. 2004 Jan;134(1):275-85. Epub 2003 Dec 4. PMID:14657410 doi:https://dx.doi.org/10.1104/pp.103.033480
- ↑ Ahlfors R, Lang S, Overmyer K, Jaspers P, Brosche M, Tauriainen A, Kollist H, Tuominen H, Belles-Boix E, Piippo M, Inze D, Palva ET, Kangasjarvi J. Arabidopsis RADICAL-INDUCED CELL DEATH1 belongs to the WWE protein-protein interaction domain protein family and modulates abscisic acid, ethylene, and methyl jasmonate responses. Plant Cell. 2004 Jul;16(7):1925-37. Epub 2004 Jun 18. PMID:15208394 doi:https://dx.doi.org/10.1105/tpc.021832
- ↑ Overmyer K, Brosche M, Pellinen R, Kuittinen T, Tuominen H, Ahlfors R, Keinanen M, Saarma M, Scheel D, Kangasjarvi J. Ozone-induced programmed cell death in the Arabidopsis radical-induced cell death1 mutant. Plant Physiol. 2005 Mar;137(3):1092-104. Epub 2005 Feb 22. PMID:15728341 doi:https://dx.doi.org/10.1104/pp.104.055681
- ↑ Fujibe T, Saji H, Watahiki MK, Yamamoto KT. Overexpression of the RADICAL-INDUCED CELL DEATH1 (RCD1) gene of Arabidopsis causes weak rcd1 phenotype with compromised oxidative-stress responses. Biosci Biotechnol Biochem. 2006 Aug;70(8):1827-31. PMID:16926493 doi:https://dx.doi.org/10.1271/bbb.50673
- ↑ Jaspers P, Blomster T, Brosche M, Salojarvi J, Ahlfors R, Vainonen JP, Reddy RA, Immink R, Angenent G, Turck F, Overmyer K, Kangasjarvi J. Unequally redundant RCD1 and SRO1 mediate stress and developmental responses and interact with transcription factors. Plant J. 2009 Oct;60(2):268-79. doi: 10.1111/j.1365-313X.2009.03951.x. Epub 2009 , Jun 22. PMID:19548978 doi:https://dx.doi.org/10.1111/j.1365-313X.2009.03951.x
- ↑ Teotia S, Lamb RS. The paralogous genes RADICAL-INDUCED CELL DEATH1 and SIMILAR TO RCD ONE1 have partially redundant functions during Arabidopsis development. Plant Physiol. 2009 Sep;151(1):180-98. doi: 10.1104/pp.109.142786. Epub 2009 Jul , 22. PMID:19625634 doi:https://dx.doi.org/10.1104/pp.109.142786
- ↑ Jaspers P, Overmyer K, Wrzaczek M, Vainonen JP, Blomster T, Salojarvi J, Reddy RA, Kangasjarvi J. The RST and PARP-like domain containing SRO protein family: analysis of protein structure, function and conservation in land plants. BMC Genomics. 2010 Mar 12;11:170. doi: 10.1186/1471-2164-11-170. PMID:20226034 doi:https://dx.doi.org/10.1186/1471-2164-11-170
- ↑ Teotia S, Lamb RS. RCD1 and SRO1 are necessary to maintain meristematic fate in Arabidopsis thaliana. J Exp Bot. 2011 Jan;62(3):1271-84. doi: 10.1093/jxb/erq363. Epub 2010 Dec 13. PMID:21172813 doi:https://dx.doi.org/10.1093/jxb/erq363
- ↑ Wirthmueller L, Asai S, Rallapalli G, Sklenar J, Fabro G, Kim DS, Lintermann R, Jaspers P, Wrzaczek M, Kangasjarvi J, MacLean D, Menke FLH, Banfield MJ, Jones JDG. Arabidopsis downy mildew effector HaRxL106 suppresses plant immunity by binding to RADICAL-INDUCED CELL DEATH1. New Phytol. 2018 Oct;220(1):232-248. doi: 10.1111/nph.15277. PMID:30156022 doi:https://dx.doi.org/10.1111/nph.15277
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